As a supplement to oral rehydration, symptomatic treatment of acute diarrhoea in infants.
The degree of rehydration by oral or intravenous rehydration solution must be adapted to the intensity
of the diarrhoea and the child’s age and specific circumstances (associated illnesses, etc.).

Oral use.
Hidrasec 10 mg is indicated in infants less than 13 kg.
Posology
The standard daily dosage is established according to body weight on the basis of 1.5 mg/kg per dose,
with a loading dose, then three doses spread throughout the day.
In practice:
Number of pouches per dose based on the infant's body weight:
• For an infant less than 9 kg: 1 pouch, 3 times daily
• For an infant weighing 9-13 kg: 2 pouches, 3 times daily.

Method of administration
The powder can be poured either onto food or into a glass of water or feeding bottle, stirring well and
ensuring that the whole of the mixture is swallowed immediately.
Day 1: Loading dose, then 3 doses spread throughout the day. On the following days: 3 doses spread
throughout the day.
Treatment must be continued until the return of two formed stools, without exceeding 7 days.

Specific populations
No studies have been conducted in children under 3 months of age.
No studies have been conducted in children with hepatic or renal insufficiency (see section 4.4).
The powder can be poured either onto food or into a glass of water or feeding bottle, stirring well and
ensuring that the whole of the mixture is swallowed immediately.

Treatment with Hidrasec is merely an adjuvant therapy in addition to oral rehydration and does not in
any way substitute it. Rehydration must be systematic in infants/children with acute diarrhoea to
prevent or treat dehydration and must be adapted in such a way as to compensate for fluid and
electrolyte losses.
Treatment of acute diarrhoea in children is primarily based on correcting fluid and electrolyte losses, by
using oral rehydration solutions and re-establishing feeding patterns as soon as possible, depending
on the child’s age and dietary habits prior to diarrhoea.
In cases of severe or prolonged diarrhoea, significant vomiting or refusal of food, intravenous
rehydration must be envisaged.
The presence of blood or pus in the stools with fever can be a sign of diarrhoea with invasive germs or
indicate the presence of other ongoing diseases. In the case of infectious diarrhoea with clinical
manifestations suggesting an invasive phenomenon, use antibacterial agents with good systemic
diffusion. Racecadotril has not been evaluated in antibiotic-associated diarrhoea. Hence, racecadotril
must not be
used in these cases.
Due to potentially reduced bioavailability, racecadotril must not be administered in cases of prolonged
or uncontrollable vomiting.
In cases of renal or hepatic insufficiency, HIDRASEC must not be administered due to the absence of
data. This medicinal product contains sucrose. Its use is not recommended in patients with fructose
intolerance, glucose-galactosemalabsorption or sucrase/isomaltase deficiency.
This medicinal product contains about 0.966 g sucrose per pouch. If the quantity of sucrose (source of
glucose and fructose) in the daily dose of this medicine exceeds 5 g per day, this must be taken into
account in the daily allowance of patients on a low-sugar diet or with diabetes.
Skin reactions have been reported with the use of this medicinal product. In most cases, these
reactions are mild and do not require any treatment. However, in certain situations, these reactions
may be severe and be life-threatening; the link with taking racecadotril cannot be entirely excluded. If
severe skin reactions appear, treatment with racecadotril must be discontinued immediately.
Cases of hypersensitivity and angioedema have been reported in patients treated with racecadotril.
These events can occur at any time during treatment.
Angioedema of the face, extremities, lips, mucous membranes may occur.
When angioedema is associated with obstruction of the upper respiratory tract, such as the tongue,
glottis and / or larynx, emergency treatment should be given immediately.
Racecadotril should be discontinued and the patient should be closely monitored with initiation of
appropriate follow-up until symptoms are completely and permanently resolved.
Patients with a history of angioedema not associated with racecadotril therapy may have an increased
risk of developing angioedema.
Concomitant use of racecadotril and ACE inhibitors may increase the risk of angioedema (see section
4.5). Therefore, a rigorous benefit-risk assessment is required before initiating treatment with
racecadotril in patients on ACE inhibitors.

Interaction of racecadotril with angiotensin-converting enzyme (ACE) inhibitors.
Risk of intensifying the undesirable effects of the angioneurotic oedema type (angioedema).

Contraindicated association:
·in case of a history of angioedema when taking an ACE inhibitor.
Association not advised:
·in the absence of a history of angioedema when taking an ACE inhibitor.

Concomitant intake of racecadotril with loperamide or nifuroxazide does not alter the kinetics of
racecadotril.

Pregnancy
Animal studies do not indicate direct or indirect harmful effects with respect to reproductive toxicity.
Clinical data on the use of racecadotril during pregnancy are very limited. As a precaution, it is therefore
preferable to avoid the use of HIDRASEC during pregnancy, regardless of the term.
Breastfeeding
In the absence of data on passage into milk and on account of its pharmacological properties and the
immaturity of the neonatal digestive tract, HIDRASEC should not be administered during breastfeeding.
Fertility
No effect on fertility has been observed during fertility studies conducted in male and female rats.

Racecadotril has no or negligible influence on the ability to drive and use machines

Clinical studies conducted on acute diarrhoea have provided safety-in-use data in 860 infants and
children treated with racecadotril and 441 treated with placebo.
The adverse reactions listed below have been observed more frequently with racecadotril than with
placebo during clinical trials, or have been reported during the post-marketing phase.
The frequency of adverse reactions has been defined according to the following convention: very
common (>1/10), common (>1/100 to <1/10), uncommon (>1/1,000 to <1/100), rare (>1/10,000 to
<1/1,000), very rare (<1/10,000), not known (cannot be estimated from the available data).
Skin and subcutaneous tissue disorders
Uncommon: rash, erythema
Not known: urticaria, angioedema (oedema of the tongue, face, lips or eyelids), erythema multiforme,
erythema nodosum, papular rash, pruritus, prurigo.

To report any side effect(s):

National Pharmacovigilance Center (NPC)
Fax: +966-1-205-7662
Call NPC at +966-11-2038222, Exts: 2317-2356-2353-2354-2334-2340.
Toll free phone: 8002490000
E-mail:npc.drug@sfda.gov.sa
Website:www.sfda.gov.sa/npc

In the cases of overdose reported, patients did not present with any undesirable effects.

Pharmacotherapeutic group: INTESTINAL ANTISECRETORY ANTIDIARRHOEAL.
ATC code: A07XA04. (A: digestive system and metabolism). 

Racecadotril is a prodrug that needs to be hydrolysed to its active metabolite thiorphan, which is an
inhibitor of enkephalinase, a cell membrane enzyme present in various tissues, including the intestinal
epithelium.
This enzyme contributes to the hydrolysis of exogenous and endogenous peptides, such as
enkephalins.
Racecadotril thus protects enkephalins from enzymatic degradation, thereby prolonging their action at
enkephalinergic synapses in the small intestine and thus reducing hypersecretion.
Racecadotril is a pure intestinal antisecretory agent. It decreases intestinal hypersecretion of water and
electrolytes induced by cholera toxin or inflammation, with no effect on basal secretion. It exerts
antidiarrhoeal activity without altering the intestinal transit time.
In two clinical studies performed in children, racecadotril reduced stool weight within the first 48 hours
by 40% and 46%, respectively.
A significant reduction in the duration of diarrhoea and the need for rehydration was also observed.
A meta-analysis (9 randomised clinical trials, racecadotril versus placebo, plus oral rehydration solution)
collected individual data from 1,384 boys and girls with acute diarrhoea of varying severity, treated in an
outpatient or hospitalised setting.
The mean age was 12 months (interquartile range: 6-39 months).
A total of 714 patients were less than 1 year old and 670 patients were more than 1 year old. The mean
weight ranged from 7.4 kg to 12.2 kg, depending on the study. The overall mean duration of diarrhoea
after enrolment was 2.81 days in the placebo group and 1.75 days for racecadotril.
In oral use, the activity of racecadotril remains peripheral without any effect on the central nervous
system.
A randomised, crossover clinical study has shown that 100 mg racecadotril at the therapeutic dose
(one capsule) or at a higher dose (4 capsules) does not induce QT/QTc prolongation in 56 healthy
adult volunteers (unlike the effect observed with moxifloxacin, used as a positive control).

Absorption:
After oral administration, racecadotril is rapidly absorbed. The activity on plasma enkephalinase
appears from the 30thminute onwards.
The bioavailability of racecadotril is not altered by food, but the activity peak is delayed by about one
and a half hours.
Distribution:
After oral administration of 14C-labelled racecadotril in healthy volunteers, the concentration of
racecadotril was about 200 times higher in the plasma than in blood cells and about 3 times higher in
the plasma than in the total blood volume. Racecadotril does not significantly bind to blood cells.
In plasma, the mean apparent volume of distribution of 66.4 kg demonstrates moderate distribution of
14C in other tissues.
Ninety percent of the active metabolite of racecadotril, thiorphan, (RS)-N-(1-oxo-2- (mercaptomethyl)-3-
phenylpropyl) glycine, is bound to plasma proteins, primarily albumin.
The pharmacokinetic properties of racecadotril are not altered during repeat-dose administration or in
the elderly.
The intensity and duration of action of racecadotril are related to the administered dose. The peak
concentration is about 2 hours 30 min., corresponding to 90% inhibition of enzymatic activity for the
administered dose of 1.5 mg/kg.
For a 100 mg dose, the duration of plasma enkephalinase activity is about 8 hours.
Metabolism:
The biological half-life of racecadotril, as determined by plasma enkephalinase inhibition, is 3 hours.
Racecadotril is rapidly hydrolysed to thiorphan (RS)-N-(1-oxo-2-(mercaptomethyl)-3-phenylpropyl)
glycine, its active metabolite, which is itself transformed into inactive metabolites S-methylthiorphan
sulphoxide, S- methylthiorphan, 2-methanesulfinylmethyl propionic acid and 2-methylsulfanylmethyl
propionic acid, which were all formed at greater than 10% systemic exposure to the parent compound.
Other minor metabolites have also been detected and quantified in urine and faecal matter. Repeated
administration of racecadotril does not induce accumulation within the body.
In vitro data show that racecadotril/thiorphan and its four major inactive metabolites have no significant
action as inhibitors of the cytochrome CYP isoforms 3A4, 2D6, 2C9, 1A2 and 2C19.
In vitro data show that racecadotril/thiorphan and its four major inactive metabolites have no significant
action as inducers of cytochrome CYP isoforms (family 3A, 2A6, 2B6, 2C9/2C19, family 1A, 2E1) and enzymes that bind to glucuronyl transferase.
Racecadotril does not alter the protein binding of highly protein-bound products, such as tolbutamide,
warfarin, niflumic acid, digoxin or phenytoin.
In patients with hepatic insufficiency (cirrhosis, Child-Pugh B), the kinetic profile of the metabolite
shows the same Tmax and T½ and lower Cmax (-65%) and areas under the curve (-29%), compared to
healthy subjects.
In patients with severe renal insufficiency (creatinine clearance between 11 and 39 mL/min), the kinetic
profile of the metabolite shows a lower Cmax (-49%) and larger areas under the curve (15%) and T½,
compared to healthy volunteers (creatinine clearance > 70 mL/min).
In the paediatric population, the pharmacodynamic results are similar to those of the adult population,
with Cmax reached 2 hours 30 minutes after administration. There is no accumulation after repeated
doses every 8 hours for 7 days.
Excretion:
Racecadotril is eliminated via its active and inactive metabolites. Elimination takes place mainly via the
kidneys (81.4%) and, to a lesser degree, via the faeces (about 8%). Excretion via the lungs is not
significant (less than 1% of the dose).

4-week chronic toxicity studies performed in monkeys and dogs, useful for the assessment of the
duration of treatment in humans, have demonstrated no effect at dosages up to 1250 mg/kg/day and
200 mg/kg, corresponding to safety margins of 625 and 62 (compared to humans), respectively.
Racecadotril has not been shown to be immunotoxic in mice treated for 1 month.
A longer duration of exposure (1 year) in monkeys showed generalised infections and reduced antibody
responses to vaccinations (at a dose of 500mg/kg/day) and no infection/immunosuppression at
120mg/kg/day.
Similarly, in dogs treated at a dose of 200 mg/kg/day for 26 weeks, some infectious/immune reactions
were detected. Their clinical significance is unknown: see paragraph 4.8.
No mutagenic or clastogenic effect of racecadotril was detected during standard tests in vivo and in
vitro. No carcinogenicity tests have been conducted, as treatment is short-term.
Reproductive toxicity and development studies (pre-embryonic development and fertility, prenatal and
postnatal development, embryofoetal development studies) revealed no particular effect of racecadotril.
A toxicity study conducted in juvenile rats showed no significant effect due to racecadotril at doses up
to 160 mg/kg/day, corresponding to a dose 35 times higher than the recommended paediatric dose
(e.g.
4.5mg/kg/day).
Despite the immaturity of renal function in children under 1 year old, higher exposure levels are not
expected in this group.
Other preclinical effects (such as severe, probably aplastic anaemia, increased diuresis, ketonuria,
diarrhoea) were observed only at exposures well above the maximum human dose. Their clinical
significance is not known.
Other safety pharmacology studies revealed no harmful effects on the central nervous system, the
cardiovascular system and respiratory functions.
In animals, racecadotril potentiates the effect of butylhyoscine on intestinal transit and the
anticonvulsant effect of phenytoin.

Sucrose

 anhydrous colloidal silica

30% polyacrylate dispersion

 apricot flavouring (vanillin, gamma undecalactone

gamma nonalactone

 allyl caproate

lemon

 neroli

 orange

 gum arabic

maltodextrin
sorbitol 

Not applicable

This medicinal product does not require any special storage conditions

1 g powder in pouches (PE/paper/aluminium); box of 16

No special requirements.
Any unused medicinal product or waste material should be disposed of in accordance with local
requirements.